The endocrine function of the fetal and neonatal rat testis has been studied with particular reference to the development and regulation of the Leydig cell and its receptor-mediated responses. The effects of gonadotropin stimulation upon fetal-neonatal Leydig cells differ markedly from those in the adult, with mainly stimulatory responses in contrast to the marked receptor loss and desensitization that is characteristic of the adult Leydig cell. A. Detailed analysis of gonadotropin receptors in the fetal rat testis revealed a close correlation between the appearance of LH receptors and gonadotropic responsiveness at 15.5 days of gestation, with a further rise at 18.5 days coincident with a marked increase in testosterone (T) production. FSH receptors appeared at 17.5 days and rose sharply after 19.5 days. These findings are consistent with the presence of Sertoli cells at this stage of gestation, and suggest that FSH has a role in gonadal development during the last 2 days of fetal life. B. In the neonatal rat, in vivo treatment with hCG elevated serum and testicular T levels with little change in progesterone and 17-hydroxyprogesterone, is contrast to the marked increase in these precursors in the adult rat. In the latter, the role of a steroidogenesic lesion in the biphasic serum T response to hCG was indicated by a marked rise in serum and testicular progesterone levels during the nadir of T production. The adult-type steroidogeic lesions that follow LH/hCG stimulation are not operative during the fetal-neonatal phase of testicular development. C. GnRH receptors were demonstrated in cultured fetal testes and neonatal gonads. In the former, expression of GnRH receptors was correlated with inhibitory effects of GnRH agonists upon LH-stimulated steroidogenesis. In the neonatal rat, GnRHa treatment markedly enhanced testicular progesterone responses to hCG or 8-BrcAMP, indicating that the adult-type steroidogenic lesion can be reproduced by GnRH acting through its Leydig-cell receptors in the neonatal testis.